ASFV Epidemiology and Global Impact

African Swine Fever Virus (ASFV) poses a significant threat to the global pig industry. Its unique DNA arbovirus properties, complex genome structure, and high pathogenicity have advanced veterinary virology research while increasing demands for detection technologies and control tools. Since its first reported outbreak in Kenya in 1921, ASFV has spread to over 50 countries, causing economic losses exceeding $100 billion. This article explores ASFV’s core biological characteristics, current research hotspots, and detection methods, providing theoretical and practical guidance for researchers.

Fig. 1 - ASF Outbreak Distribution Map (Jan 2022 - Jul 2025). Source: WOAH website.

ASFV Structure and Key Antigens

The uniqueness of ASFV stems from its complex structure, genome, and host interaction mechanisms, influencing detection targets and control strategies.

Multilayered Virus Structure

ASFV particles exhibit icosahedral symmetry with a diameter of 200–300 nm. The core components include linear double-stranded DNA and key proteins, central to research and detection:

• Capsid Protein p72 (B646L gene): Forms the main capsid component with high sequence conservation, serving as the gold standard for ASFV genotyping (24 genotypes identified). Its epitope stability enables cross-strain detection.
• Early Expression Protein p30 (CP204L gene): Expressed within 6 hours post-infection in macrophages, ideal for early infection screening and differentiating latent from acute infections.
• Envelope Glycoprotein CD2v (EP402R gene): Mediates adhesion to red blood cells (haemadsorption) and is key for tissue tropism and immune evasion, making it a candidate for vaccine development.
• Metabolic-Related Proteins (A238L, p54/pE183L): A238L aids viral nucleic acid replication, while p54 facilitates envelope fusion with host cell membranes. Both are critical for studying replication and auxiliary detection.

Fig. 2 - ASFV Structure. Source: DOI: 10.3389/fimmu.2021.715582.

Genome Characteristics and Mutation Mechanisms

The ASFV genome (170–193 kbp) encodes 150–200 open reading frames (ORFs). Mutations occur primarily in variable regions at genome ends, driven by recombination in multigene families (MGF):

• MGF Genes (e.g., MGF360, MGF505): Show significant strain variation, aiding host adaptation and immune evasion. The 2024 I/II recombinant strains, with low virulence and high transmissibility, result from MGF gene recombination, challenging single-genotype detection assays.
• Core Functional Genes (e.g., p72, p30): Relatively conserved, but point mutations in strains like EU Genotype IX and Asian recombinants may reduce antibody binding efficiency, necessitating broad-spectrum reagents.

Pathogenesis: Immune Suppression

ASFV primarily infects pig mononuclear macrophages, employing a “precise invasion + immune suppression” strategy:

• Entry via CD2v protein binding to CSF2RA receptors on macrophages, releasing the genome.
• Independent replication using encoded DNA polymerase and topoisomerase (e.g., pP1192R), while MGF360-16R inhibits type I interferon signaling, blocking antiviral responses.
• Late-stage induction of macrophage apoptosis and cytokine storms, causing high fever, hemorrhaging, organ failure, and 90%–100% mortality in acute infections.

Fig. 3 - Model of ASFV Transcription Dual Systems. Source: DOI: 10.1038/s41467-024-54461-1.

Research Hotspots: Mutation Mechanisms and Vaccine Development

ASFV research focuses on mutation mechanisms, vaccine development, and host interactions, supporting innovative prevention and detection technologies.

Molecular Mechanisms of Recombinant Strains

Recombinant I/II strains, characterized by low virulence and high transmissibility, are a key focus:

• Recombinant Fusion Region Analysis: CRISPR/Cas9-based studies show MGF505 and MGF360 fusion fragments enhance host cell binding and reduce immune recognition.
• Immune Evasion Mechanisms: Techniques like CoIP and SPR identify proteins (e.g., K196R) binding to macrophage HSP60, inhibiting apoptosis and offering potential inhibitor targets.

Vaccine Development Strategies

Vaccine research centers on live attenuated and subunit vaccines, relying on antigen and antibody tools:

• Live Attenuated Vaccines: Constructed via gene knockout (e.g., MGF360/505), with anti-pp62 antibodies verifying immunogenicity post-attenuation.
• Subunit Vaccines: Combine p72 and CD2v with nano-carriers and adjuvants, using ELISA to measure neutralizing antibody titers (e.g., anti-p30), with some candidates achieving over 85% protection in trials.
• mRNA Vaccines: Optimize p72 and p30 sequences, using Western Blot to confirm antigen expression and immunogenicity.

Common Detection Targets and Methods

abinScience ASFV Research Tools

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